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Neo Vita - Human Reproduction and Reproductive Health

Technical Manager: Dr. Fernando P. Ferreira

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Endometriosis

TRUTHS AND MYTHS

According to recent studies, endometriosis affects approximately 12% of women of reproductive age. Only in our country has about 6 million carriers.

One of its most striking features is an evolutionary character, that is, it begins with superficial injuries, easily treatable, and progresses to severe conditions as in deep intestinal endometriosis, when the treatment becomes much more complex. It is therefore essential that the diagnosis is made as early as possible.

Unfortunately, it occurs across the planet, an average interval of time, from the first symptoms to the diagnosis, from approximately 7 years.

For this reason, reports have been advising women to seek out a specialist as soon as they start experiencing cramps or pain in their sexual relations. On the other hand, we have observed a worrying phenomenon. Inaccurate information or personal testimonials transmitted causing panic to thousands of women. In this process, two stand out and deserve urgent clarification.

It is often said that endometriosis has no cure. However, when a woman is treated, either through medications or laparoscopy, and the lesions are all removed, we can say that it is completely healed. That causes this confusion is the fact that once with endometriosis, there is a marked propensity to have it again, which it inevitably happens if the woman continues to menstruate as before, without medication. With proper treatment at disease hardly returns.

The second piece of information that deserves to be reviewed is the common impression that rare women with endometriosis manage get pregnant. Recent studies indicate that about 60% of affected women will be able to conceive without difficulty. The remaining 40%, in fact, must undergo treatment, either through videolaparoscopy or reproduction techniques assisted as in vitro fertilization.

DEEP INTESTINAL ENDOMETRIOSIS

 

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Deep intestinal endometriosis affects 10 to 30% of affected women. This form of the disease can cause mild symptoms with mild or moderate menstrual cramps. In others it causes severe symptoms including cramps pain, pain during bowel movement and infertility. According to the most modern studies, not all patients with deep endometriosis by surgery. Treatment should be individualized after careful clinical evaluation, transvaginal ultrasound with intestinal preparation or magnetic resonance.

CLINIC TREATMENT:

When clinical treatment is chosen, hormonal methods such as combined pills are available, which combine estrogen and progesterone, or the progestogen pills. Other options are injectables, adhesives, vaginal ring or IUD levonorgestrel releaser. GnRH analogs are also important options for the treatment of endometriosis intestinal but should be used for a short period due to side effects.

SURGERY:

The surgery is performed through videolaparoscopy and aims to eliminate all injuries, bringing the pelvic organs to their normal anatomy. This procedure requires complex hospital structure, specific equipment and staff used to this type of procedure. Many women believe that these surgeries lead to a colostomy frequency. It is important to explain that this happens in less than 1% of surgeries for deep intestinal endometriosis. For the complete extraction of the lesions, it may be necessary to remove a small intestinal segment. In these cases, the presence of a specialist in gastrosurgery is mandatory.

HOW ENDOMETRIOSIS CAUSES INFERTILITY

Endometriosis is a chronic disease, associated with pelvic pain and infertility. The prevalence rate of endometriosis has estimated at 5-10% in women of reproductive age. Around 25-50% of women with infertility can be affected by endometriosis and about 30-50% of women with endometriosis have infertility.

It is caused by the growth of endometrial tissue outside the uterine cavity, which induces a chronic inflammatory reaction dependent on estrogen, which is the hormone responsible for the growth of endometriosis lesions.

This tissue can also grow in small superficial parts, being called implants. Some women they may have few implants that don’t grow, or the disease can spread through the entire pelvis. In the presence of Endometrial implants also cause the release of prostaglandins (PG), substances involved with the mechanism of pain and that allow the appearance of adhesions with different degrees of distortion in the anatomy of the pelvis. The implants can also lead to bleeding in the surrounding structures, which causes pain and the development of more pelvic adhesions.

Many women who have endometriosis have few symptoms, or may be asymptomatic symptom (not having any symptoms). But we also have symptomatic ones. Severe menstrual pain, pain during intercourse and pain to evacuate or will urinate the most frequently reported symptoms.

The most affected sites are the pelvic organs and the peritoneum (tissue that covers the organs). The most frequent are: ovaries, fallopian tubes, uterus sacral ligaments, (which fix the uterus in the spine), uterus, bladder, ureter and intestine. But Endometriosis can also affect other distant organs, such as the diaphragm, lungs, skin, scars and even the brain.

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ENDOMETRIOSIS CLASSIFICATION:

According to the American Society for Reproductive Medicine (ASRM), endometriosis is classified into 4 clinical stages and in 4 types:

Stage I: minimum

Stage II: mild

Stage III: moderate

Stage IV: severe

Type I – Superficial / peritoneal: Foci of lesions affecting the peritoneum;

Type II – Endometrioma: Cysts are formed with dark brown content (chocolate);

Type III – Deep / infiltrative: The endometriotic lesions extend more than 5 mm below the peritoneum infiltrating

in the organs. It is responsible for painful symptoms, the severity of which is strongly correlated with the depth of the lesions, forming nodules behind the cervix, ureters, vagina, intestine and others.

Type IV – Adenomyosis: When endometriosis affects the muscular layer of the uterus (myometrium).

Classification in stages has a descriptive function as to the number and locations of injuries and has no relation to symptom sand intensity of the patient’s pain.

ENDOMETRIOSIS CAUSE:

The cause of endometriosis remains unknown. However, there are several theories that try to explain the origin of the dispersed endometrial lesions that occur in women with endometriosis. Theories are: menstruation retrograde, celomic metaplasia and lymphatic / hematogenous dissemination.

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In the 1927s, Sampson proposed the most accepted theory, called retrograde menstruation, which consists of the exit of menstrual flow to the pelvic cavity through the fallopian tubes. Retrograde menstruation occurs when the flow menstrual cycle containing fragments of the endometrium is transported in a retrograde manner through the fallopian tubes to the peritoneal cavity during menstruation with subsequent implantation in the peritoneum and ovary. According to this theory, endometrial cells can implant themselves on the ovaries or anywhere in the pelvic cavity. This theory gained support with the findings of greater volume of reflux blood and endometrial tissue in the pelvis of women with endometriosis.

CELOMIC METAPLASIA:

The theory of celomic metaplasia can also contribute to the understanding of the development of endometriosis.During the first weeks of pregnancy, the reproductive organs are developed from embryonic leaflets specifics. The theory postulates that metaplasia of the celomic epithelium is the origin of endometriosis because cells of the peritoneum visceral and endometrial are both derived from the same embryonic precursor. Thus, the epithelium of the celoma which in embryonic life gave rise to the endometrium and the ovarian germinal epithelium remain in the pelvic peritoneum, with the potential for endometrial metaplasia, thus creating foci of endometriosis. It is a supported theory for ovarian endometriosis. The celomic epithelium that covers the ovary and the serosa of the peritoneum may undergo a change metaplastic in the endometrium.

That is, the woman is born with the endometrium outside the normal location (which would be inside the uterus) and this endometrium is active, developing endometriosis.

According to this theory, it is not the endometrium that comes from retrograde menstruation that generates endometriosis, but a tissue that has already is out of place since birth.

LYMPHATIC/ HEMATOGENIC DISSEMINATION:

The theory of lymphatic / hematogenous dissemination is associated with the infiltrating endometrial tissue that can form metastases through the lymphatic vessels or the vascular system, which could be attributed to implants found outside the pelvic cavity. This theory would explain the presence of fragments of endometrium that, when penetrating in lymphatic vessels and blood, would justify endometriotic foci found in distant and rare places, such as the lungs (pleura), bones, skin. Therefore, it does not explain the location of implants that have more common locations.

PHYSIOPATHOLOGICAL MECHANISM IN INFERTILITY:

Endometriosis has a negative impact on fertility, since the presence of ectopic endometrial implants (outside the uterine cavity) is associated with anatomical distortions, which can cause obstruction in the fallopian tubes and adhesions that they prevent the transport of the oocyte until it meets the sperm. Changes occur in the peritoneal fluid that interfere with fertilization, ovulatory disorders, follicular and embryonic changes, by producing substances and inflammatory cells. Because it is an estrogen dependent disease, there are implantation disorders due to changes in endometrium by local production of estrogen and resistance to progesterone.

EFFECT ON OOCYTES, EMBRYO AND ENDOMETRY

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Folliculogenesis (growth and development of the follicle for egg production) is impaired in women with endometriosis. The number of preovulatory follicles, follicular growth, dominant follicle size and concentrations of hormones within the follicle are reduced in the ovaries of patients with endometriosis. The follicular fluid of patients endometriosis has been reported to have changes in hormonal profiles, including reduced estrogen, progesterone and androgen and the increase in a substance called of ativin. In addition, the follicular fluid of patients with Endometriosis has been shown to have inflammatory substances, such as cytokines and growth factors that could promote the maintenance of endometriosis injuries.

The quality of sperm is also reduced by the inflammatory and toxic effects and the increase in macrophages activated in the peritoneal fluid, which literally “eat” (phagocytize) the sperm. Increasing the number of cells inflammatory reactions in the peritoneal fluid not only damage oocytes and sperm, but have also been shown to have toxic on the embryo. There is also a disorder in the luteal phase (phase of the menstrual cycle that occurs after ovulation) that happens due to the dysregulation of the progesterone receptor, as well as an effect on the target genes of progesterone, which in turn leads to a decrease in endometrial receptivity (ability of the embryo to implant in the uterus).

In addition, studies have demonstrated the aberrant expression of antioxidant enzymes, glutathione peroxidase and catalase in the endometrium of endometriosis patients and it can be suspected that there is also an increase in free radicals of the endometrium and subsequently a negative effect on the embryo’s vitality. These abnormalities and the inflammatory substances released in the pelvic peritoneum can contribute to the loss of oocyte and embryo quality, increasing the abortion rate due to impaired implantation.

PREGNANCY AND BORN FEES

Infertile patients with mild endometriosis have a spontaneous pregnancy rate of 2% to 4.5% per month, incompared to a monthly fertility rate of 15% to 20% in normal couples. Infertile patients with moderate and severe endometriosis have monthly pregnancy rates below 2%. Laparoscopic treatment of Minimal and mild endometriosis has been associated with a small but significant improvement in pregnancy rates. Second studies, to date, 29% of women who have had endometriosis treated have achieved pregnancy within nine months. In vitro fertilization (IVF) is the most effective treatment for moderate to severe endometriosis, particularly if not there is restoration of fertility through laparoscopic surgery.

For the IVF procedure, the treatment success rate is similar to the other causes of infertility, so it varies a lot depending on the age of the woman, as over the years there is a natural loss of eggs both in quantity as in quality.

Therefore, birth rates are approximately:

42% for women under 35;

32% between 35 and 37 years old;

22% between 38 and 40 years;

12% between 41 and 42 years old.

PRESENCE OF ENDOMETRIOMA

Endometrioma is a term used when endometriosis affects the ovaries, developing cysts that are detected by transvaginal ultrasound. The endometrioma have a liquid inside, the content is bloody with chocolate color, due to the presence of endometrial cells inside the ovary.

This cyst is shaped by cells of the endometrium that detach and adhere to the ovaries. In addition to causing pain in endometrioma may also prejudice folliculogenesis, affecting ovarian reserve and fertile potential.

Several studies have been performed with goal to investigate the effect of ovarian endometrioma on the ability of the ovaries to respond to the stimulus and results of in vitro fertilization (IVF). Thus, these indicated that presence of ovarian endometrioma reduces the number of oocytes recovered (in terms of their oocyte quality), developed embryos quality, implantation rate and clinical pregnancy. Due to endometrioma, changes in the factors occur immune systems such as IL-6 accumulation or silencing of vascular endothelial growth factor in follicular fluid and these were considered negative for follicular growth and oocyte maturation. It is relevant to approach that it isn’t presence of the endometrioma itself, which causes low responsiveness to the ovaries, but the deleterious effect on the microenvironment of endometriosis, such as inflammation and production of reactive oxygen species.

In conclusion, the treatment of endometrioma depends on the size of the cyst and the severity of the symptoms. Can be performed using hormonal medications or laparoscopic surgery, indicated when the cysts are larger 3cm and symptoms are plentiful. Therefore, studies suggest that surgical removal of endometrioma before IVF offers no benefit for successful treatment, as there is a loss in ovarian reserve and assisted human reproduction would provide a therapeutic approach to infertility related to endometrioma instead of laparoscopic ovarian surgery in asymptomatic patients.

REFERENCES IN MEDICAL LITERATURE

  • American Society for Reproductive Medicine (ASRM). Fact Sheets and Info Booklets – Endometriosis. 2007.
  • American society for reproductive medicine. A guide for patients. Endometriosis 2012.
  • Burney and Giudice., Pathogenesis and Pathophysiology of Endometriosis. Fertil Steril, 2012.
  • Chapron et al.,Deeply infiltrating endometriosis: pathogenetic implications of the anatomical distribution. Human reproduction, 2006.
  • Harris-glocker, miranda; mclaren, janet f. Role of female pelvic anatomy in infertility. Clinical anatomy, v.1, n. 26, p.89-96, 2013.
  • Stilley, julie a. W.; birt, julie a.; sharpe-timms, kathy l.. Cellular and molecular basis for endometriosis-associated infertility. Cell tissue res, v. 349, n. 3, p.849-862, 03 fev. 2012.
  • Vercellini et al., Endometriosis: pathogenesis and treatment. Nature reviews and endocrinology, 2014.
  • Yang et al., Impact of ovarian endometrioma on ovarian responsiveness and IVF: a systematic review and meta-analysis. Reproductive BioMedicine Online, 2015.

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